The nervous system includes the Central Nervous System (CNS) and the Peripheral Nervous System (PNS), the latter including the Somatic Nervous System (SNS) and Autonomic Nervous System (ANS). The CNS includes the brain and the spinal cord. The spinal cord is the main communication route for signals between the body and the brain. The PNS carries signals outside the brain and spinal cord throughout the rest of the body, including carrying motor signals to muscles and carrying sending feedback to the brain, including touch and pain signals from the skin. The SNS and ANS overlap the CNS and PNS. There are 31 pairs of spinal nerves arising from cervical (8), thoracic (12), lumbar (5), sacral (15) and coccygeal (1) segments. The spinal nerves contain both sensory and motor fibers. Efferent nerves (as opposed to afferent nerves) are the nerves leading from the central nervous system to an effector organ, and efferent neural outflow refers to neural signals from the brain that are transmitted via spinal cord pathways to effector organs.
The SNS is the part of the peripheral nervous system associated with the voluntary control of movement via the Skeletal muscles. The ANS consists of two divisions, the sympathetic nervous system and the parasympathetic nervous system, and is responsible for regulating bodily functions including heart rate, respiration, digestion, bladder tone, sexual response and other functions. Activation of the sympathetic nervous system results in preparation of the body for stressful or emergency situations, while activation of the parasympathetic nervous system results in conservation and restoration and controls body processes during normal situations. The autonomic nervous system includes both sensory and motor neurons. Preganglionic neurons start in the CNS and project to a ganglion in the body where they connect with postganglionic neurons that connect with a specific organ.
There are many disorders and dysfunctions associated with abnormal regulation of effector organs, which may be due to disturbances in any component of the nervous system. These effector organs can be skeletal muscles under voluntary control, smooth muscle under autonomic control, or visceral organs and glands. We have developed a novel approach to modulating these systems using trans-spinal direct current stimulation (tsDCS).
Muscle tone abnormalities are associated with many neurological pathologies and can severely limit motor function and control. Muscle tone depends on the level of excitability of spinal motoneurons and interneurons. Muscle tone abnormalities can be due to either decreased tone (hypotonus) or increased tone (hypertonus). Hypotonia is commonly observed, for example, in patients with cerebellar deficits and spinocerebellar lesions and in developmentally-delayed children, including those with Down's syndrome. Hypertonia is commonly observed, for example, in patients with cerebral palsy, stroke, spinal cord injury (SCI), brain injury, multiple sclerosis and numerous other neurological disorders. Hypertonia includes spasticity and rigidity and is characterized by a velocity-dependent increase in tonic stretch reflexes and increased muscle activity during passive stretch. Spasticity can range from mild to severe and can cause striking impairments in functional movement. There is a long felt need for better ability to control and regulate muscle tone. Spinal cord injury is one indication where an increase in muscle tone is often seen.
Increases in reflex excitability following SCI may be caused by a number of factors, including increased excitability of spinal motoneurons and changes in interneuronal physiology and connectivity. In general, following SCI, increased excitation and reduced inhibition of the mechanisms controlling motoneurons causes abnormal generation of force, resulting in spasticity. Pharmacological, surgical, and physical treatments to manage spasticity have at best short-term efficacy and are confounded by side effects.
Beyond skeletal muscle disorders, there are numerous disorders related to dysfunction of either the sympathetic or parasympathetic system that have been described. These ANS disorders are referred to as dysautonomias, and can be due to failure or disruption of either the sympathetic or parasympathetic divisions of the ANS. Specific such disorders include familial dysautonomia, autoimmune autonomic ganglionopathy, congenital central hypoventilation syndrome, Holmes-Adie syndrome, multiple system atrophy, Shy-Drager syndrome, neurally mediated syncope, orthostatic hypotension, postural tachycardia syndrome, striatonigral degeneration and vasovagal syncope. No effective treatments currently exist for these dysautonomias. A novel approach to autonomic neuromodulation would not only open new treatment options for these patients, but would enable the harnessing of the autonomic nervous system to modulate the activity of all the organ systems innervated autonomically.
There remains a need for improved method and apparatus for neuromodulation and regulation of effector organs.